Evidence map›Paper›PMID 8169593›Full record

ArticleThe Journal of general physiology1994

Regulation of cAMP-activated apical membrane chloride conductance in gallbladder epithelium.

T A Heming, J Copello, L Reuss

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. A primary culture of guinea pig gallbladder epithelial cells that is responsive to secretagogues.American journal of physiology. Gastrointestinal and liver physiology · 2000
    Article
  4. Stretch-activated single K+ channels account for whole-cell currents elicited by swelling.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  5. Article
  6. Electrogenic cation transport across leech caecal epithelium.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 1996
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

T A HemingDepartment of Physiology, University of Texas Medical Branch, Galveston 77555.
J Copello
L Reuss
The University of Texas Medical Branch at Galveston · US

Funding

NIDDK NIH HHS DK-38784
6 · The paper itself

Abstract

Regulation of the cAMP-activated apical membrane Cl- conductance (GaCl) in Necturus gallbladder (NGB) epithelial cells was investigated with intracellular-microelectrode techniques. GaCl was increased by exposure to 8-Br-cAMP, theophylline or forskolin. Neither 8-Br-cGMP nor elevation of intracellular [Ca2+] using ionomycin had effects on GaCl or interfered with activation of GaCl by forskolin. N-(2-[methylamino]ethyl)-5-isoquinolinesulfonamide (H8), an inhibitor of cAMP-dependent protein kinase (PKA), slowed but did not prevent the GaCl response to 8-Br-cAMP. Phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC), stimulated GaCl but had no effects on intracellular [cAMP]. GaCl was unaffected by 4 alpha-phorbol, a PMA analog which does not activate PKC. Okadaic acid (OA), an inhibitor of protein phosphatases (PP) types 1 and 2A, slowed the activation of GaCl by 8-Br-cAMP, hastened the return of GaCl to basal values following removal of 8-Br-cAMP, and significantly reduced the elevation in intracellular [cAMP] produced by forskolin. OA had no effects on the GaCl changes elicited by theophylline. We conclude that: (a) NGB GaCl can be activated by PKA-mediated phosphorylation of apical membrane Cl- channels or a regulatory protein, (b) GaCl can also be activated via PKC, by a cAMP-independent mechanism, (c) OA-sensitive PP are not required for inactivation of GaCl; OA appears to stimulate phosphodiesterase, which lowers intracellular [cAMP] and affects GaCl activation, and (d) the apical membrane of NGB epithelium lacks a Ca(2+)-activated Cl- conductance.

Indexed as

AnimalsCalciumChloride ChannelsColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMPElectrophysiologyEnzyme ActivationEpitheliumEthers, CyclicGallbladderIn Vitro TechniquesIonomycinMembrane PotentialsNecturus8-bromocyclic GMPCalciumChloride ChannelsColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMPEthers, CyclicIonomycinOkadaic AcidPhosphoprotein PhosphatasesProtein Kinase CTheophylline

Identifiers

PMID8169593
PMCPMC2216856
OpenAlexW2105631751

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.